Three Is Flashcards
Ischemia
Coronary artery supplies the heart with blood and can be gradually Narrowed by lipid deposits that become atheromatous plaques beneath the intima lining of the vessel. The intima may eventually rupture exposing the plaque to the blood with in the artery initiating immediate formation of a clot. Decrease in blood supply ( hypoxia )it is recoverable and characterizes a partial blockage in the coronary artery, can cause chest pain without infarction. In EKGs it is seen as T-wave inversion That is symmetrical (if biphasic should start w/ negative deflection) can vary from slight to deep ( blood flow can decrease without producing in infarction (checking leads V1through V6 to see if there is diminished coronary flow) and ST segment depression Measured 0.08 sec after end of QRS greater than or equal to -1mV or one box for the depth of the St-segment depression may slope down or be flat can be with or without t wwave inversion. Ischemia and injury are always acute
Ischemia – Inverted T waves, ST Depression
–decrease in blood supply (hypoxia)
–acute, short term, transient
–Problem: stable plaque narrows artery; demand (e.g., exercise) exceeds supply
–Tissue not injured, but recovers following removal of ischemia
Injury
The vessel narrowed by plaque can become occluded by the thrombus causing instant infarction of the ventricle and can become necrotic. Ventricular foci in the hypoxic area around the infarction become irritable producing deadly ventricular arrhythmias. Most commonly develops in the left ventricle given its size and oxygen demand suffers from obstruction the most. The heart is Damaged blood flow stopped for too long. Injury indicates the acuteness ( New or recent ) of an infarct, with or without loss of R wave and localizes anatomically. In EKGs it is characterized by ST elevation ( slight or up to 10 mm above baseline ) current of injury . Angina with exertion, prinzmetals angina can cause transient ST elevation in the absence of an infarction. With or without loss of R wave. Ischemia and injury are always acute
Injury – ST Elevation
–damage
–(transmuralischemia): acute, longer-term, ischemia (minutes in duration)
–Problem: demand > supply even at rest for prolonged period
Often caused by unstable plaque
Infarction
Necrosis due to obstruction of blood supply. Clot completely including area. in EKGs it is characterized by Q wave peaking with increased pulling of the ST segment up in elevation after four minutes of damage, with or without T wave changes = myocardial injury Myocardial infarction results from the complete occlusion of a coronary artery the infected area of myocardium becomes necrotic so it can’t do you polarize or contract. Presence of a Q wave indicates infarction. Which are produced by an area of necrosis in the wall of the left ventricle. Note which leads have significant Q waves omit leave a VR . Significant Q waves ≥ 0.04 sec or 1/3 the amplitude of QRS, –Insignificant q waves are < 0.04 sec, Localize anatomically
Infarction – Q Waves
–necrosis due to obstruction of blood supply.
Q waves not going away means old only signifcantw/ ischemia and injury, if alone old
Acute or old, where it is, which of the three Is
T waves in MIs
T waves usually are positive in leads I, II, and V3to V6, and negative in aVR. They can be variable in appearance in the rest of the leads normally are assymetric . Flat or nonexistent he wears or minimal T-wave inversion may be a normal variant for a limb leads. However T-wave inversion in the chest leads is pathological (V2-V6, normal in frontal): usually symmetrical can cuase angina . Do you even version in Leeds the two and three are hallmark of Welland syndrome alerting us to stenosis of the LAD artery. Symmetrical T waves found in pathological states such as: Ischemia, Electrolyte abnormalities, CNS problems and Symmetrical T waves can be normal in SOME people, but should be considered pathological until proven otherwise.
Tall, peaked, symmetrical narrow T waves (midprecordial leads) are common in hyperkalemia or ischemia. Very broad T waves have been found in CNS events, especially intracranial hemorrhage.
To determine symmetry:
- Place your hairline ruler vertically on the peak of the T wave (shown on the next slide).
- If the two sides separated by the dividing line are mirror images, the T wave is symmetrical. If not, it is asymmetrical.
If you have difficulty evaluating the ST segment, extend the two legs of the T wave as a straight line down to the baseline (shown on next slide).
ST segment: depression and elevation
Electrically, the ST segment represents the section of the complex in which the ventricles are between electrical depolarization and repolarization.
The segment is measured from the J point (where the QRS complex and ST segment meet) to the beginning of the T wave.
In most instances, the measurement is an approximation, either because the J point is not sharp or because the beginning of the T wave is not clearly visible.Two little boxes over from the J point 1 mm difference in order to be significant.
Prinzmetals angina- can cause transient ST elevation in the absence of an infarction. Can also cause Angina with exertion, ST segment elevation is the earliest EKG sign of an infarction. with time treatment, the ST segment returns to baseline. If the ST segment is elevated without associated Q waves this may be non-Q wave infarction a small infarction heralding and impending larger one. Ventricular aneurysm ( outward ballooning of the wall of a ventricle) can cause persistent ST elevation in most chest leads the ST segment will not return to baseline with time. Perry carditis produces a unique a type of ST I meant elevation can elevate T-wave off of the baseline. ST changes in V one and we too are always significant and important both depression and elevation.
ST depressions: Can be due to subendocardialinfarction, stress test, digitalis
Brugada
Hereditary condition that can cause sudden death and individuals without heart disease characterized by Right bundle branch pattern QRS with ST elevation in V one through V3 can lead to sudden cardiac arrest in the absence of coronary obstruction, Peculiar peaked downsloping shape in V1 enV2 caused by dysfunctional sodium channels in the heart. With prophylaxis against deadly arrhythmias requiring defibrillator implant Tatian to treat
Perry carditis
ST segment is elevated and usually flat or concave. Entire T-wave elevated off baseline. Inflammation of the pericardium membrane surrounding heart. Maybe caused by a virus bacteria cancer or am I. Resolved with time elevating the entire T-wave off the baseline angling back down including the P-wave to the next QRS. PVCs can be produced
Sub endocardial infarction
And infarct that does not extend through the full thickness of the left ventricular wall without infarction affecting only a small area of myocardium just beneath the endocardial lining. Is a true am I the requires care can in large or extend and become more life-threatening most MIs are transmural or the full thickness of the wall . When a patient with narrowed coronary arteries exercises the myocardium demands more blood flow then the arteries can deliver. ST segment may become flattened ( horizontal or downsloping ) and depressed under certain circumstances or conditions such as a positive stress test or digitalis. Any significance as he depression in the lead to where the QRSs upright indicates compromised coronary blood flow warranting further investigation
Insignificant Q waves
Ventricular depolarization begins midway down the interventricular septum. Septal depolarization initiated at mid septum by the left bundle branch goes from left to right pattern with the initial right where the ventricle killer activation producing tiny insignificant or small Q waves and lead to where the QRS is upright that are less than 0.4 seconds and 1 mm. Right bundle branch transverses septum vertically without branching but the left bundle branch gives off terminal Purkinje fiber is at the mid septum
Significant Q waves
At least one small square wide 0.3 seconds (more significant measurementor 1/3 of the entire QRS amplitude indicating the necrosis of a myocardial infarction.
Ignore aVR
Ignore isolated Q’s in V1
Ignore isolated Q’s in III
Ignore Q’s in LBBB
More reliable if found with ischemia or injury
Less reliable if LVH is present
Must meet size criteria first
Anterior infarction
Positive chest leads to record only initial away vectors from the opposite side recording a Q wave . Q waves in V1 V2V3V4 are indicators. Interior portion of the left ventricle include part of the interventricular septum. When isolated Q waves appear In V1 and V2 infarction includes a septum or anteroseptal infarction. Isolated key waves in V3 and V4 which are more laterally located represent anterolateral infarction. Insignificant Q waves are normally in leads five and six. Acute-anteroseotal anterior infarction produces Q waves and ST elevation in V1&V2. Anterior infarction is due to the occlusion of the left anterior descending branch of the left coronary artery.
Lateral infarct
Positive left arm electrode records only initial away vectors from the opposite side recording a Q wave through the void of the necrotic lateral infarct . Positive electrode use to record lateral limb leads one and a VL on the left arm . If Q waves in these leads there is a lateral left ventricular infarction. Lateral infarction caused by an occlusion of the circumflex branch of the left coronary artery.
Inferior infarct
Diagnosed by the presence of Q waves in the inferior leads to three and AVF check ST segment to see if infarction is a cute. Resting upon diaphragm and is in relation to the right ventricle called the diaphragm Mattick infarction. Positive left arm electoral records only initial away vectors from the opposite side recording a Q wave
. Base of the left ventricle receives its blood supply from the branches of the right or left coronary artery. Does not necessarily identify the artery Blanche that is occluded unless you have a previous x-ray toy Denna five which artery supplies the inferior portion of the patients ventricle. Left or right coronary dominance the notes which coronary artery is the major source of blood supply to the left ventricle with right coronary dominance most common
Left ventricular depolarization during infarction
Left ventricular depolarization moves in opposite directions simultaneously in opposing walls. Perking to fibers conduct so rapidly that depolarization is initiated in all endocardial services lining the left ventricle at the same time depolarization passes from endocardium to epicardium. Depolarization of the anterior wall and the posterior wall of the left ventricle are in opposite directions depolarization of the anterior wall of the left ventricle proceed from the inner endocardium lining ventricle through the full thickness of the ventricular wall to the outer surface of the epicardium.
Posterior infarction
A cute post Siri infarction there is a large our way opposite of a Q wave in B1 and B2. In lead V1 a Q wave turned upside down would look like in R wave suspect true post your infarction when you see this even though right ventricular hypertrophy can also produce this. ST depression opposite of ST elevation of injury in V1 or V2. If you suspect an acute posterior infarction ( large R waves and ST depression and V1 or V2): You was reversed transillumination inverting the EKG tracing then holding so that it faces a strong light observing the backside of the tracing to check for Q waves and ST depression in the inverted V one and week two ladie you was reversed transillumination inverting the EKG tracing then holding so that it faces a strong light observing the backside of the tracing to check for Q waves and ST depression in the inverted V1 and V2 leads; mirror test inverted EKG tracing observe it in the mirror, if there is an acute post your infarction you will see classic signs of Q waves an ST elevation in the reflection of the inverted leads. True posterior infarctions caused by an occlusion of the right coronary artery or its branches supplying the SA node, AV node in the Hess bundle. Causing serious arrhythmias
Left bundle branch block infarctions
And left bundle branch block the ventricle the main Chabert to suffer infarction D polarizes after the right ventricle. Any Q wave originating in the left ventricle could not appear at the beginning of the QRS complex with the left bundle branch rather it would be somewhere in the middle of the complex. The right and left ventricles share the interventricular septum so an infarct in the Seattle area would be shared by the right ventricle, which depolarizes first in the left bundle branch block. Producing Q waves at the beginning of the wide curious which would suggest but not confirm i and left bundle branch block the ventricle the main Chabert to suffer infarction D polarizes after the right ventricle. Any Q wave originating in the left ventricle could not appear at the beginning of the QRS complex with the left bundle branch rather it would be somewhere in the middle of the complex. The right and left ventricles share the interventricular septum so an infarct in the Seattle area would be shared by the right ventricle, which depolarizes first in the left bundle branch block. Producing Q waves at the beginning of the wide curious which would suggest but not confirm in nfatction
Tombstone segment
T waves that are flipped and symmetrical
**Indicates large myocardial infarction**
Progression in infarct
The ECG patterns in AMI are not a static picture, but rather a continuum that extends from the normal state to a full infarct, as shown in this image.
The first thing that happens is that the T wave flips in early ischemia.
Next, there is ST elevation that is either flat or tombstoning. The flipped T wave may disappear for a short time during this stage.
Finally, we start to see Q waves.
When acute infarct is over, the chronic pattern of old infarct begins to develop.
The first thing to disappear is ST segment elevation, with return of the segment to the baseline. ischemia
The T wave then reverts to upright.- injury
The Q wave remains permanently because of scar formation- infarcation.The infarct pattern may take weeks to resolve to this level.
